Bilateral symmetry is a common feature of nervous system anatomy across phylogeny. Morphological symmetry is contrasted by the lateralization of many different nervous system functions, likely caused by individual cell types adopting different fates and functions along the left/right (L/R) axis. The molecular mechanisms of creating cellular diversity along the L/R axis in the nervous system are, however, poorly understood. The nervous system of the nematode Caenorhabditis elegans displays several examples of lateralization, including the L/R asymmetry displayed by the two ASE taste receptor neurons, ASE left (ASEL) and ASE right (ASER). While bilaterally symmetric in regard to all known morphological criteria, these two neurons display distinct chemosensory capacities which correlate with the L/R asymmetric expression of three putative chemoreceptors. We aim to understand how L/R asymmetric cell fate is created in the ASEL and ASER neurons. We hypothesize that L/R asymmetry is induced by a signal of unknown molecular nature. We propose to use laser ablation to identify the cellular source of the signal (Aim #1) and we propose to understand the molecular nature of the signal by characterizing mutants which we isolated from a genetic screen for L/R asymmetry defects (Aim #2). Our previous genetic analysis has already revealed a cascade of gene regulatory factors (including homeobox genes and miRNAs) that act in ASEL and ASER to diversify their respective fates. Future genetic studies will determine how the asymmetric activity of these gene regulatory factors is triggered. Our studies may provide novel insights into the creation of cellular diversity in the nervous system.